ArticleHypertension research : official journal of the Japanese Society of Hypertension2020
A potential role of caspase recruitment domain family member 9 (Card9) in transverse aortic constriction-induced cardiac dysfunction, fibrosis, and hypertrophy.
Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Exacerbation by knocking-out metallothionein gene of obesity-induced cardiac remodeling is associated with the activation of CARD9 signaling.International journal of biological sciences · 2025Article
- Macrophage OTUD1-CARD9 axis drives isoproterenol-induced inflammatory heart remodelling.Clinical and translational medicine · 2024Article
- Macrophage CARD9 mediates cardiac injury following myocardial infarction through regulation of lipocalin 2 expression.Signal transduction and targeted therapy · 2023Article
- More than just a small left ventricle: the right ventricular fibroblast and ECM in health and disease.American journal of physiology. Heart and circulatory physiology · 2023Review
- Triptolide promotes autophagy to inhibit mesangial cell proliferation in IgA nephropathy via the CARD9/p38 MAPK pathway.Cell proliferation · 2022Article
- CARD9 Regulation and its Role in Cardiovascular Diseases.International journal of biological sciences · 2022Review
- Annual reports on hypertension research 2020.Hypertension research : official journal of the Japanese Society of Hypertension · 2022Review
- CARD9 Signaling, Inflammation, and Diseases.Frontiers in immunology · 2022Review
- CARD9: key player or bystander in cardiac remodeling under hypertension?Hypertension research : official journal of the Japanese Society of Hypertension · 2020Article
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9 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Macrophage- and monocyte-derived cytokines are elevated in the myocardium of pressure-overloaded hearts, where they play critical roles in pathological remodeling. Caspase recruitment domain family member 9 (CARD9) regulates macrophage cytokine secretion, but its role in a transverse aortic constriction (TAC) model of pressure overload has not been evaluated. To investigate whether CARD9 may serve as a valuable therapeutic target, wild-type (WT) and CARD9-knockout mice were subjected to 3 months of TAC, and then cardiac function, hypertrophy, and fibrosis were analyzed. The expression of protein markers of myocardial autophagy and nuclear factor kappa B signaling was also investigated. At 1 month after TAC, cardiomyocyte contractile dynamics were measured in a separate cohort to further assess contractility and diastolic function. In WT but not CARD9
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